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Survival (p < 0.0001). Thus, CNKSR1 expression status might capture unfavorable tumor biology for surgical resection for pancreatic cancer, and may aid in pre-operative treatment selection.Quadri et al. BMC Cancer (2017) 17:Page 7 ofTable 1 Characteristics of patients included in the studyAll Patients (N = 120) Age group
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Pathologists (MM, MA). CNKSR1 low (0 and 1 + expression) versus CNKSR1 high (2+, 3+) comprised 28.3 and 71.7 of cases in the study cohort and 44.1 and 55.9 of cases in the validation cohort suggesting similar expression patterns across the different arrays. In the study cohort 30 of cases also showed some degree of nuclear staining (Fig. 5b). Nuclear staining was lower than cytoplasmic expressi
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Patients for individualized clinical decision-making would fill an unmet clinical need. Activating somatic KRAS mutations are nearly omnipresent and a hallmark in the genetic make-up of pancreatic ductal adenocarcinoma (PDAC) [5]. While KRAS mutations themselves have been associated as prognostic markers, there is considerable and significant heterogeneity in the activation states of the downstrea
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Survival (p < 0.0001). Thus, CNKSR1 expression status might capture unfavorable tumor biology for surgical resection for pancreatic cancer, and may aid in pre-operative treatment selection.Quadri et al. BMC Cancer (2017) 17:Page 7 ofTable 1 Characteristics of patients included in the studyAll Patients (N = 120) Age group
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Survival (p < 0.0001). Thus, CNKSR1 expression status might capture unfavorable tumor biology for surgical resection for pancreatic cancer, and may aid in pre-operative treatment selection.Quadri et al. BMC Cancer (2017) 17:Page 7 ofTable 1 Characteristics of patients included in the studyAll Patients (N = 120) Age group
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Patients for individualized clinical decision-making would fill an unmet clinical need. Activating somatic KRAS mutations are nearly omnipresent and a hallmark in the genetic make-up of pancreatic ductal adenocarcinoma (PDAC) [5]. While KRAS mutations themselves have been associated as prognostic markers, there is considerable and significant heterogeneity in the activation states of the downstrea
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S. Increased CNKSR1 expression levels were observed in tumor tissues compared to matched normal tissue by Wilcoxon matchedpairs signed rank test (** p = 0.004)Table 1 presents demographic and clinical characteristics of the pancreatic cancer patient specimens used for clinical outcome associations (SEER, UMD, and NIH). Table 2 presents the demographics and tumor characteristics by CNKSR1 expressio